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Multiple Sclerosis: Back to Basics

Discussion in 'General Issues and Discussion Forum' started by NewsBot, Jun 3, 2013.

  1. NewsBot

    NewsBot The Admin that posts the news.

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    Press Release:
    Multiple sclerosis: Back to basics?
    Link to article: http://f1000.com/prime/reports/m/5/20/
     
  2. Admin2

    Admin2 Administrator Staff Member

  3. Mr C.W.Kerans

    Mr C.W.Kerans Active Member

    I had an unfortunate female patient who had rapidly progressive MS, with severe muscle spasm who in consequence had trouble with an IGTN - ingrown toenail - (left 1st). She went on to develop leukaemia, and while in hospital for chemotherapy, she developed an acute IGTN. The dilemma faced was if the IGTN was not remedied, and her compromised immune system led to infection, her chemo schedule would have been interupted. If need arose to use LA in treating the ingrown toenail, nobody could advise me if the LA would be effective - I still don't know. In the event, conservative measures were successful; she sadly died from the leukaemia. Does anybody have any views on this unusual situation?
     
  4. NewsBot

    NewsBot The Admin that posts the news.

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    Press Release:
    MS Treatment Options Growing, Raising New Hope, Loyola Neurologist Reports
    'Rapid expansion' of medications for Multiple Scerlosis
     
  5. NewsBot

    NewsBot The Admin that posts the news.

    Articles:
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    Press Release:
    First study to investigate the human genome in multiple sclerosis
    The National Institutes of Health awarded Benaroya Research Institute at Virginia Mason $1.9 million to find marks in the human genome which can explain why some white blood cells cause damage to the spinal cord and brain in multiple sclerosis
     
  6. NewsBot

    NewsBot The Admin that posts the news.

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    Press Release:
    Research reveals new understanding, warning signs, and potential treatments for multiple sclerosis
     
  7. NewsBot

    NewsBot The Admin that posts the news.

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    Press Release:
    FDA approves new MS treatment regimen developed at Wayne State University
    Higher dose, fewer injections for patients around the world

     
  8. NewsBot

    NewsBot The Admin that posts the news.

    Articles:
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    Press Release:
    Antibody May Be Detectable in Blood Years Before MS Symptoms Appear
     
  9. NewsBot

    NewsBot The Admin that posts the news.

    Articles:
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    Stem cell treatment halts MS progression in 91% of patients

    High-Dose Immunosuppressive Therapy and Autologous Hematopoietic Cell Transplantation for Relapsing-Remitting Multiple Sclerosis (HALT-MS)
    A 3-Year Interim Report

    Richard A. Nash et al
    JAMA Neurol. Published online December 29, 2014
     
  10. NewsBot

    NewsBot The Admin that posts the news.

    Articles:
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    Press Release:
    How multiple sclerosis can be triggered by brain cell death
    Nanoparticles stop the progressive disease and are being developed for humans
    Surprise finding: death of cells that make myelin can initiate MS
    Nanoparticles prevent progressive MS in animal model
    "Intervening early in disease will have greatest impact"
     
  11. NewsBot

    NewsBot The Admin that posts the news.

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    Press Release:
    Breakthrough may stop multiple sclerosis in its tracks
     
  12. NewsBot

    NewsBot The Admin that posts the news.

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    Rehabilitation in Multiple Sclerosis: a Systematic Review of Systematic Reviews
    Fary Khan, MBBS, MD, FAFRM (RACP), Bhasker Amatya, MD, MPH
    Archives of Physical Medicine and Rehabilitation; in press
     
  13. NewsBot

    NewsBot The Admin that posts the news.

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    FDA News Release
    FDA approves Zinbryta to treat multiple sclerosis
    For Immediate Release
    May 27, 2016
     
  14. NewsBot

    NewsBot The Admin that posts the news.

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    Press Release:
    Multiple sclerosis: Newly discovered signal mechanism causes T cells to turn pathogenic
     
  15. NewsBot

    NewsBot The Admin that posts the news.

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    PUBLIC RELEASE: 9-JAN-2017
    Breakthrough in MS treatment
    Drug shown to reduce new attacks/symptom progression in some patients

     
  16. NewsBot

    NewsBot The Admin that posts the news.

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    PUBLIC RELEASE: 8-FEB-2017
    Study sheds light on the biology of progressive form of multiple sclerosis
    Suggests a new potential path for treatment
     
  17. NewsBot

    NewsBot The Admin that posts the news.

    Articles:
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    The Effects of Tai Chi on Physical and Psychosocial Function among Persons with Multiple Sclerosis: A Systematic Review
    Emily Taylor, , Ruth E. Taylor-Piliae
    Complementary Therapies in Medicine 2 March 2017
     
  18. NewsBot

    NewsBot The Admin that posts the news.

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    PUBLIC RELEASE: 20-JUL-2018
    A molecular key for delaying the progression of Multiple Sclerosis is found

    Multiple Sclerosis is an autoimmune disease that attacks and destroys a structure known as the "myelin sheath", whose integrity is indispensable for the brain and spinal cord to function properly.

    Current treatment of Multiple Sclerosis is based on modulating the activity of the immune system or preventing its cells from accessing the central nervous system and damaging it. These therapies are effective in the early phases of the disease, but they do not prevent its advance and the progressive functional deterioration.

    During the progressive phase of the disease it is the microglial cells in the brain that are the main cause of the chronic inflammation responsible for the neurological deterioration. These microglial cells are the brain's sentries and react when faced with any damage or infection in it. This reaction, which is in principle beneficial, becomes harmful when it is prolonged over time, leading to chronic inflammation, and aggravates the disease and encourages its progression.

    In the work just published it was possible to identify a receptor known as P2X4 present in the microglial cells that increases their anti-inflammatory potential in order to reduce the damage in Multiple Sclerosis and, above all, encourage the body's own repair responses.

    This experimental development was conducted using animal models of this disease, thanks to which it was possible to discover that the drugs that activate this receptor improve the symptoms during the chronic phase of the disease when furthering the repair of the nervous tissue.

    As Dr María Domercq of the UPV/EHU's Department of Neurosciences and who works at the ACHUCARRO centre for research in Leioa (Basque Country) pointed out, "We are witnessing a discovery that is opening up a new channel of pharmacological development for the treatment of the progressive phase of Multiple Sclerosis, and with it we want to open a new door on improving the life quality of people who suffer Multiple Sclerosis".

    This ambitious study was developed by an international research group coordinated from the Basque Autonomous Community, specifically from Leioa, with research personnel from the ACHUCARRO research centre, the UPV/EHU, ciberNed and CICbiomaGUNE in collaboration with the technical contribution of professionals from the University of Hamburg in Germany, and the Institut de Génomique Fonctionnelle in Montpellier, France.
     
  19. NewsBot

    NewsBot The Admin that posts the news.

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    PUBLIC RELEASE: 22-JAN-2019
    Multiple sclerosis -- Helping cells to help themselves
    Researchers decipher one of the body's brain regeneration mechanisms


    Diseases such as multiple sclerosis are characterized by damage to the 'myelin sheath', a protective covering wrapped around nerve cells akin to insulation around an electrical wire. Researchers from Charité - Universitätsmedizin Berlin have discovered how the body initiates repair mechanisms which will limit the extent of any damage to this sheath. Their findings, which provide a basis for the development of new drugs to treat multiple sclerosis, have been published in the eminent journal Nature Communications*.

    Multiple sclerosis is the most common autoimmune disease of the central nervous system. Estimates suggest that more than 200,000 people are affected by the disease in Germany alone. People with multiple sclerosis experience vision and sensory problems, as well as impaired coordination or even paralysis. These symptoms are caused by the disruption of nerve impulses in either the brain or the spinal cord. This disruption occurs when the body's immune system attacks the myelin sheath, which is wrapped around the body's nerve fibers and provides electrical insulation. When the myelin sheath is no longer intact, communication between nerve cells is impaired. Researchers across the globe are searching for new ways to repair the myelin sheath and, in doing so, are looking to reduce neurological symptoms in people with multiple sclerosis. Researchers from Charité have now moved a decisive step closer to this goal.

    Charité's research team decided to take a closer look at the body's innate ability to heal itself, knowing that, under certain conditions, the central nervous system is capable of repairing damage to the myelin sheath. Specific molecular signals enable stem cells to differentiate into myelin repair cells (oligodendrocytes), which reside in a small stem-cell niche in the brain. Once they leave this niche, these repair cells migrate to where myelin damage has occurred in order to restore the affected nerve cells' electrical insulation. Until now, very little had been known about the molecular signals responsible for initiating this myelin regeneration mechanism. "We have found that the Chi3l3 protein plays a central role in the body's capacity to produce new myelin-forming oligodendrocytes," says the study's first author, Dr. Sarah-Christin Staroßom of Charité's Institute for Medical Immunology. A researcher at the NeuroCure Cluster of Excellence and the Experimental and Clinical Research Center (ECRC), Dr. Staroßom explains the protein's role as follows: "The Chi3l3 protein initiates the differentiation of neural stem cells into myelin repair cells, which restore the electrical insulation around damaged nerve cells."

    Using a mouse model, the research team were able to show that a reduction in Chi3l3 levels in the brain significantly impairs the body's capacity for oligodendrocyte production, while a Chi3l3 infusion leads to an increase in the production of myelin repair cells. The same reaction was observed during an in vitro experiment using human cells. "We hope to use this knowledge to develop a new generation of drugs that can be used in the treatment of multiple sclerosis," explains Dr. Staroßom. "As a next step, we will study in greater detail whether Chi3l3 or related proteins can be used to reduce the neurological symptoms of patients with multiple sclerosis."
     
  20. NewsBot

    NewsBot The Admin that posts the news.

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    PUBLIC RELEASE: 24-JAN-2019
    Multiple sclerosis: Perilous ruptures

    The permanent neurological deficits of multiple sclerosis patients largely depend on the extent of degeneration of long nerve fibers. The latter is initiated by ruptures in the cell membrane and the resulting influx of calcium ions.

    In Germany alone, more than 200,000 patients suffer from multiple sclerosis (MS). MS is an autoimmune condition and one of the most common inflammatory diseases of the central nervous system. The degree of the patient´s disability, is critically dependent on the extent of nerve-fiber loss. This is because the autoimmune reaction characteristic of the condition attacks the long processes, called axons, which are responsible for the transmission of nerve impulses. Now a team led by Professor Martin Kerschensteiner, Director of the Institute of Clinical Neuroimmunology at Ludwig-Maximilians-Universitaet (LMU) in Munich, and Professor Thomas Misgeld of the Institute for Neuronal Cell Biology at the Technical University of Munich (TUM), working with an animal model of MS has identified a putative mechanism that can result in the degeneration of axons. They have shown that minuscule ruptures in the cell membrane allow calcium ions to percolate into the neuron, disrupting the ionic balance and ultimately killing the axon. The new findings appear in the journal Neuron.

    In previous studies, Kerschensteiner, Misgeld and colleagues had observed that axons in inflammatory lesions often were swollen and subsequently fragmented. "But in some cases, the swelling spontaneously regressed and these axons recovered," says Kerschensteiner. "So the process is in principle reversible, and could perhaps be therapeutically modulated if we had a better understanding of the underlying mechanisms." With the aid of in-vivo microscopy, the researchers have now shown in an animal model of MS that the fate of these axons depends on their calcium content. Axons with an abnormally high concentration of calcium are more likely to undergo swelling and subsequent degeneration and less likely to recover from this state than axons with normal levels of the ion. "Strikingly, these changes begin relatively early in the course of the axon damage process," says Misgeld. Indeed, in 10% of the axons examined, the calcium concentration was already increased prior to the onset of swelling. About half of the swollen axons were found to have high levels of intracellular calcium, and a correspondingly high risk of degeneration.

    The excess calcium is derived from the extracellular space and it enters the axon via nanoruptures in the cell membrane, as the team was able to demonstrate using a fluorescent dye coupled to a macromolecule. "The complex is too large to penetrate into an intact axon. Only if the membrane has been damaged can it be taken up into the axon and detected by its fluorescence. With the aid of in-vivo microscopy, we were also able to show that many of the axons that take up the dye also contain increased amounts of calcium," says Kerschensteiner. "The fact that, in the inflamed nervous system, tears in the cell membrane can contribute to the death of nerve fibers is a new discovery, which could in future be therapeutically relevant." adds Misgeld. It is already known from studies of spinal cord injury that nerve cells have the capacity to repair ruptures caused by mechanical forces. The researchers therefore hope that a better understanding of the origins and repair of damaged nerve-cell membranes will bring them closer to identifying new targets for therapeutic interventions.
     
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